98%
921
2 minutes
20
Background: Alzheimer's disease is a neurodegenerative condition characterized by memory deficits and cognitive decline. Ivermectin, an antiparasitic agent, has shown neuroprotective effects. The present study was conducted to determine the protective effects of ivermectin in a streptozocin-induced Alzheimer's model in rats.
Methods: Alzheimer's model was induced by bilateral intracerebroventricular injection of streptozocin (3 mg/kg BW, 2 doses). Ivermectin was administered intraperitoneally at a dose of 2 mg/kg. On day 19, after behavioral memory and learning tests, the samples were collected for histological and enzymatic studies.
Results: Ivermectin reduced the histopathological changes, including pyknotic and dead neurons and the accumulation of Aβ plaques. Ivermectin administration also reduced serum ( < 0.0001) and brain tissue ( < 0.01) acetylcholinesterase activity as well as improved learning ( < 0.05) and spatial memory ( < 0.0001).
Conclusions: Ivermectin demonstrates protective effects in the STZ-induced Alzheimer's model by reducing pathological changes and Aβ plaques, acetylcholinesterase activity, as well as improving memory and learning.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1080/17582024.2025.2554374 | DOI Listing |
Lab Chip
September 2025
Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, USA.
Traumatic brain injuries (TBIs) are a risk factor for Alzheimer's disease (AD), and share several important pathological features including the development of neurofibrillary tangles (NFT) of tau protein. While this association is well established, the underlying pathogenesis is poorly defined and current treatment options remain limited, necessitating novel methods and approaches. In response we developed "TBI-on-a-chip", an trauma model utilizing murine cortical networks on microelectrode arrays (MEAs), capable of reproducing clinically relevant impact injuries while providing simultaneous morphological and electrophysiological readout.
View Article and Find Full Text PDFNeuroinflammation has emerged as a central and dynamic component of the pathophysiology underlying a wide range of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Far from being a secondary consequence of neuronal damage, inflammatory processes (mediated by microglia, astrocytes, peripheral immune cells, and associated molecular mediators) actively shape disease onset, progression, and symptomatology. This review synthesizes current knowledge on the cellular and molecular mechanisms that govern neuroinflammatory responses, emphasizing both shared and disease-specific pathways.
View Article and Find Full Text PDFActa Neuropathol Commun
September 2025
Department of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, 58185, Linköping, Sweden.
Disruptions in synaptic transmission and plasticity are early hallmarks of Alzheimer's disease (AD). Endosomal trafficking, mediated by the retromer complex, is essential for intracellular protein sorting, including the regulation of amyloid precursor protein (APP) processing. The VPS35 subunit, a key cargo-recognition component of the retromer, has been implicated in neurodegenerative diseases, with mutations such as L625P linked to early-onset AD.
View Article and Find Full Text PDFMethods Cell Biol
September 2025
Histology and Cell Biology Department, School of Medicine, Complutense University of Madrid, Madrid, Spain. Electronic address:
Parkinson disease (PD) is the second most prevalent neurodegenerative disorder globally, trailing only Alzheimer´s disease. It currently affects nearly 3 % of individuals aged 65 and above. The disease is characterized by the progressive loss of dopaminergic neurons accompanied by a chronic neuroinflammatory process, which is responsible for both motor symptoms (tremor, rigidity, bradykinesia) and non-motor symptoms (depression, dysphagia, anxiety, constipation, and anosmia).
View Article and Find Full Text PDFMethods Cell Biol
September 2025
Department of Physiology, Medical School, National and Kapodistrian University of Athens, Athens, Greece. Electronic address:
Mitochondrial dysfunction is a shared hallmark of neurodegenerative disorders, including Alzheimer's disease (AD) and tauopathies among others. Pathological alterations of the microtubule-associated protein Tau can disrupt mitochondrial dynamics, transport, and function, ultimately leading to neuronal toxicity and synaptic deficits. Understanding these processes is crucial for developing therapeutic interventions.
View Article and Find Full Text PDF